Histochemical and electron microscopic observations on the myoneural junctions of rats with carbon disulfide induced polyneuropathy.

Huang

Acta Neurologica Scandinavica

et al. 1996

We report the clinical features, electrophysiological studies, sural nerve pathology and recovery course of carbon disulfide-(CS2) induced polyneuropathy in a 48-year-old man who worked in a viscose rayon plant. Sural nerve biopsy 2 years later still showed degeneration of both axon and myelin with a predominant loss of large myelinated fibers and remyelination. Electrophysiologic studies revealed mixed axonal and demyelinating polyneuropathy. To our knowledge, this is the first human report of sural nerve pathology in the recovery stage due to CS2 intoxication. After diagnosis, the patient was removed from the toxic environment. In the following three years, he showed part recovery predominantly in motor function compatible with the serial nerve conduction studies. We conclude that CS2 polyneuropathy may partly recover years after cessation of exposure.

Section: Carbon Disulfide Polyneuropathysupporting

confidence: 93%

Section: Carbon Disulfide Polyneuropathysupporting

confidence: 86%

Section: Carbon Disulfide Polyneuropathymentioning

confidence: 99%

See 1 more Smart Citation

Carbon disulfide induced polyneuropathy: sural nerve pathology, electrophysiology, and clinical correlation

Huang

Acta Neurologica Scandinavica

et al. 1996

American J Industrial Med

“…Possibly, a more direct toxic interference with CS 2 metabolism in the nervous system rather than a vasculopathy may have resulted in the more diffuse encephalopathy seen in our group. A direct toxic effect of CS 2 on peripheral nerve cells and myoneural junctions has been demonstrated in experimen tal animals [Juntunen et al, 1977;Szendzikowski et al, 1973]. Other studies on experimental animals have given indications of disturbances in copper metabolism, enzyme inhibition with depressing effects on mitochondrial metabolism, and distur bances of brain catecholamine metabolism [Scheel, 1967;Tarkowski and Sobczak, 1971;Magos, 1975].…”

Section: Discussionmentioning

confidence: 99%

Carbon disulfide exposure and neurotoxic sequelae among viscose rayon workers

Aaserud

Hommeren

Tvedt

et al. 1990

In Norway's only viscose rayon plant, carbon disulfide (CS2) concentrations in ambient air usually were between 30 and 50 mg/m3 during the first 23 years of production. From 1970/1971 until the factory was closed in 1982, corresponding values were 10-25 mg/m3. Through all of these years, high peak exposures of CS2 and H2S occurred. In 1986, 16 of the 24 men still at work in 1982 and with at least 10 years' experience in the spinning room agreed to participate in this study. Clinical neurological examination demonstrated abnormalities in 15; neuropsychological tests showed impairments of probable organic origin in 14. Thirteen had cerebral atrophy demonstrated by cerebral computed tomography (CT). Electromyography (EMG) was abnormal in six, neurography in 11. Regional cerebral blood flow measurements indicated flow asymmetries in eight, whereas Doppler investigation of the extracranial carotid and vertebral arteries, electroencephalography (EEG), and evoked response investigations were mostly normal. Based on these results and the exposure data, a diagnosis of CS2-induced encephalopathy was reached in eight workers; another six had an encephalopathy in which CS2 exposure was regarded as a partial cause. Correspondingly, seven had a neuropathy probably caused by CS2 exposure alone; in three others, CS2 was found to be the partial cause of a neuropathy. This indicates that long-term, relatively moderate exposure to CS2 in association with high peak exposures to CS2 and H2S involves a substantial risk of developing neurotoxic disease.

Ultrastructure of carbon disulphide neuropathy

Jirmanová

Lukás²

1984

Acta Neuropathol

Adult Wistar rats were exposed to carbon disulphide (CS2) vapour at a concentration of 2.4 mg/l of air for 5 days a week (6 h a day), and the ultrastructure of peripheral nerves, neuromuscular junctions and muscles was investigated after 6 months of exposure to CS2. Numerous giant axons, i.e. paranodal or internodal swellings, were seen in the peripheral nerves. At the swollen paranodes, the myelin sheath was thinned, in other regions large intramyelinic vacuoles indicative of more dramatic demyelination were observed at axonal enlargements. Axonal enlargements consisted essentially of whorls of tightly packed neurofilaments. A number of nerve fibres underwent complete degeneration, but at the same time there was evidence of nerve regeneration. Nerve terminals were affected in a similar way following CS2 exposure. At neuromuscular junctions, filamentous swellings of nerve terminals preceded their degeneration and eventual denudation of synaptic gutters. As a rule, the postsynaptic part of neuromuscular junctions remained unimpaired by CS2 treatment. Muscles were affected by both atrophy and degeneration. Clusters of dense and lamellar bodies and numerous autophagosomes indicative of direct myotoxic effect of CS2 were frequently encountered in the investigated muscles. Some muscle fibres apparently underwent necrosis judging from the occurrence of myotubes characteristic of muscle degeneration and regeneration. The pathomorphology of CS2 neuropathy resembles that of other toxic neuropathies which presumably have a common origin in impaired energy metabolism.